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171.
172.
Human granulosa cells were maintained in culture with extracellular matrix
in the presence or absence of human chorionic gonadotrophin (HCG) using a
defined culture medium. Such cultures are maintained by gonadotrophin in a
manner suggesting that features of 'luteal rescue' may be occurring in
vitro. Western analysis of culture medium demonstrated that the granulosa
cells produced tissue inhibitor of metalloproteinases (TIMP)-1 but not
TIMP-2. The presence of TIMP-1 in cultured cells was also detected
immunocytochemically. Immunoassay of TIMP-1 output revealed that HCG
exposure for 7 days caused a 2-fold increase in TIMP-1 production versus
control reaching maximum at approximately 1 ng HCG/ml. The sensitivity of
this response to HCG was similar to that observed for stimulation of
progesterone production. Delayed addition of HCG, from day 4 of culture,
elicited increases in TIMP-1 which were evident within 24 hours, and were
not explained by changes in cell replication or survival. Removal of HCG
from cultures previously luteinized with HCG for 6 days resulted in a fall
in TIMP-1 production. Thus TIMP-1 production by luteinized granulosa cells
in culture is gonadotrophin dependent. We speculate that prolonged cellular
function associated with 'luteal rescue' may result from increased
extracellular matrix stability mediated by up-regulation of TIMP-1
production.
相似文献
173.
The survival motor neuron protein in spinal muscular atrophy 总被引:19,自引:1,他引:19
Coovert DD; Le TT; McAndrew PE; Strasswimmer J; Crawford TO; Mendell JR; Coulson SE; Androphy EJ; Prior TW; Burghes AH 《Human molecular genetics》1997,6(8):1205-1214
The 38 kDa survival motor neuron (SMN) protein is encoded by two
ubiquitously expressed genes: telomeric SMN (SMN(T)) and centromeric SMN
(SMN(C)). Mutations in SMN(T), but not SMN(C), cause proximal spinal
muscular atrophy (SMA), an autosomal recessive disorder that results in
loss of motor neurons. SMN is found in the cytoplasm and nucleus. The
nuclear form is located in structures termed gems. Using a panel of
anti-SMN antibodies, we demonstrate that the SMN protein is expressed from
both the SMN(T) and SMN(C) genes. Western blot analysis of fibroblasts from
SMA patients with various clinical severities of SMA showed a moderate
reduction in the amount of SMN protein, particularly in type I (most
severe) patients. Immunocytochemical analysis of SMA patient fibroblasts
indicates a significant reduction in the number of gems in type I SMA
patients and a correlation of the number of gems with clinical severity.
This correlation to phenotype using primary fibroblasts may serve as a
useful diagnostic tool in an easily accessible tissue. SMN is expressed at
high levels in brain, kidney and liver, moderate levels in skeletal and
cardiac muscle, and low levels in fibroblasts and lymphocytes. In SMA
patients, the SMN level was moderately reduced in muscle and lymphoblasts.
In contrast, SMN was expressed at high levels in spinal cord from normals
and non- SMA disease controls, but was reduced 100-fold in spinal cord from
type I patients. The marked reduction of SMN in type I SMA spinal cords is
consistent with the features of this motor neuron disease. We suggest that
disruption of SMN(T) in type I patients results in loss of SMN from motor
neurons, resulting in the degeneration of these neurons.
相似文献
174.
Nicolino MP; Puech JP; Kremer EJ; Reuser AJ; Mbebi C; Verdiere-Sahuque M; Kahn A; Poenaru L 《Human molecular genetics》1998,7(11):1695-1702
175.
176.
177.
Intravenous calcitriol regresses myocardial hypertrophy in hemodialysis patients with secondary hyperparathyroidism 总被引:1,自引:0,他引:1
CW Park YS Oh YS Shin CM Kim YS Kim SY Kim EJ Choi YS Chang BK Bang 《American journal of kidney diseases》1999,33(1):73-81
To evaluate the response of circulating intact parathyroid hormone (iPTH) on myocardial hypertrophy in hemodialysis (HD) patients with secondary hyperparathyroidism (SHPT), echocardiographic and neurohormonal assessments were performed over a 15-week period in 15 HD patients with SHPT before and after calcitriol treatment and 10 HD control patients with SHPT not receiving calcitriol therapy. We prospectively studied a group of 15 patients with significantly elevated iPTH levels (iPTH >450 pg/mL) receiving calcitriol (2 microg after dialysis twice weekly). Clinical assessment, medication status, and biochemical and hematological measurements were performed once a month. Throughout the study, calcium carbonate levels were modified to maintain serum phosphate levels at less than 6 mg/dL, but body weight, antihypertensive medication, and ultrafiltration dose remained constant. In patients treated with calcitriol, an adequate reduction of iPTH levels was found (1,112 +/- 694 v 741 +/- 644 pg/mL; P < 0.05) without changes in values of serum ionized calcium (iCa++), phosphate, or hematocrit. Blood pressure (BP), cardiac output (CO), and total peripheral resistance (TPR) did not significantly change. After 15 weeks of treatment with calcitriol, M-mode echocardiograms showed pronounced reductions in interventricular wall thickness (13.9 +/- 3.6 v 12.8 +/- 3.10 mm; P = 0.01), left ventricular posterior wall thickness (12.5 +/- 2.4 v 11.3 +/- 1.8 mm; P < 0.05), and left ventricle mass index (LVMi; 178 +/- 73 v 155 +/- 61 g/m2; P < 0.01). However, in control patients, these changes were not found after the treatment period. In addition, sequential measurements of neurohormonal mediator levels in patients receiving calcitriol showed that plasma renin (18.5 +/- 12.7 v 12.3 +/- 11.0 pg/mL; P = 0.007), angiotensin II (AT II; 79.7 +/- 48.6 v 47.2 +/- 45.7 pg/mL; P = 0.001), and atrial natriuretic peptide (ANP; 16.6 +/- 9.7 v 12.2 +/- 4.4 pg/mL; P = 0.03) levels significantly decreased, whereas antidiuretic hormone (ADH), epinephrine, and norepinephrine levels did not change significantly. The percent change in LVMi associated with calcitriol therapy had a strong correlation with the percent change in iPTH (r = 0.52; P < 0.05) and AT II (r = 0.47; P < 0.05) levels. We conclude that the partial correction of SHPT with intravenous calcitriol causes a regression in myocardial hypertrophy without biochemical or hemodynamic changes, such as heart rate, BP, and TPR. The changes in plasma levels of iPTH and, secondarily, plasma levels of neurohormones (especially AT II) after calcitriol therapy may have a key role in attenuating ventricular hypertrophy in SHPT. 相似文献
178.
179.
180.
Kibbelaar RE; Mulder JW; Dreef EJ; van Kamp H; Fibbe WE; Wessels JW; Beverstock GC; Haak HL; Kluin PM 《Blood》1993,82(3):904-913
Fluorescence in situ hybridization (FISH) is a powerful tool for detection of numerical and structural chromosomal aberrations. We have compared conventional banding techniques and FISH for the detection of monosomy 7 (-7) and trisomy 8 (+8) in 89 patients with myeloid malignancies. Of these patients, 21 had -7, 30 had +8, four had both, and 34 had no aberrations or aberrations other than -7 or +8 as assessed by banding techniques. Sequential samples were available in 23 patients. Alphoid DNA probes specific for chromosomes no. 7 and 8 were used for FISH. As controls, 10 normal bone marrow (BM) samples were hybridized with the chromosomes no. 7 and 8 probes, and in addition all tumor samples were hybridized with a chromosome no. 1 specific probe. The cut-off value for -7 was 18% one-spot cells, and for +8 was 3% three-spot cells. FISH analysis of 44 samples with -7 or +8, and at least 10 metaphases evaluated, showed that the proportions of aberrant metaphase cells mirrored the interphase clone sizes. Most samples with nonclonal metaphase aberrations, including those with only a few metaphases, had increased numbers of aberrant interphase cells: 20% to 80% for -7, and 3% to 43% for +8. Interphase cytogenetics of the 34 samples without -7 or +8 did not show significant cell populations with -7 or +8. In four patients, -7 or +8 could not be confirmed by FISH due to additional structural aberrations, marker chromosomes, or wrongly interpreted banding results. As FISH will be used more and more in cytogenetic diagnosis, clinical follow-up, and therapy monitoring, it will be necessary to standardize FISH procedures and supplement the Standing Committee on Human Cytogenetic Nomenclature (ISCN) definitions of a clone with criteria specifically for in situ hybridization. 相似文献